Wu C W, Chung W W, Chi C W, Kao H L, Lui W Y, P'eng F K, Wang S R
Department of Surgery, Veterans General Hospital-Taipei, Taiwan.
Virchows Arch. 1996 Aug;428(6):325-31. doi: 10.1007/BF00202199.
High levels of arginase have been detected in gastric adenocarcinoma. To examine the hypothesis that this is due to macrophage infiltration into the tumour, we localized the cellular distribution of arginase by immunohistochemical staining. We examined gastric adenocarcinomas and their corresponding normal tissues (n = 45), leiomyomas (n = 2), leiomyosarcomas (n = 3), human gastric adenocarcinoma cell lines (n = 3), and benign gastric ulcers (n = 4) by the avidin-biotin-peroxidase complex technique. Macrophages with strong arginase immunoreactivity were observed infiltrating both gastric normal and cancer tissues. No arginase immunoreactivity was observed in normal mucosal gland, muscular and serosal tissues or benign gastric ulcers. The immunoreactivity of arginase was positive but heterogeneous in most specimens of gastric adenocarcinoma (62.2%) and was absent from gastric intestinal metaplasia, leiomyomas and leiomyosarcomas. Among the 28 neoplasms with arginase immunoreactivity, scattered immunoreactivity was also noted in adjacent dysplastic glands in 12 (42.8%) specimens. Arginase immunoreactivity was observed in all three gastric cancer cell lines. Arginase is present in the cytoplasm but not in the nucleus. These data suggest that the high arginase levels in adenocarcinoma cancer tissues originate largely from cancer cells.
